Acute Kidney Injury Fact Sheet Clinical Issues

Total Page:16

File Type:pdf, Size:1020Kb

Acute Kidney Injury Fact Sheet Clinical Issues Developed by: ANNA Specialty Practice Networks Acute Kidney Injury Fact Sheet Clinical Issues Overview • Overuse of medications, such as nonsteroidal anti- inflammatory drugs (NSAIDs, such as ibuprofen, With over 30 definitions of acute kidney injury (AKI) in pub- naproxen) and angiotension-converting enzyme (ACE) lished studies, there is no consensus among experts inhibitors. regarding how AKI is defined (Palevsky et al., 2013). Palevsky and colleagues (2013) describe AKI as a sudden Intra-Renal or Intrinsic loss of kidney function occurring over hours to days, result- Direct injury to the kidney or renal parenchyma due to fac- ing in fluid and electrolyte imbalance, retention of nitroge- tors, such as: nous waste products in the blood, and acid base irregular- • Cancer. ity. More specifically, AKI is defined as an increase in serum • Systemic Infection or sepsis. creatinine of 0.3 m/dL or higher within 48 hours, or an • Interstitial nephritis or allergic reaction to medications. increase in serum creatinine 1.5 times baseline within the • Scleroderma or other connective tissue disorder. prior 7 days, or a decrease in urine volume less than 0.5 • Damage to the renal tubules, such as glomerulonephri- mL/kg/hr for 6 hours (Kidney Disease: Improving Global tis, vasculitis, or thrombotic microangiography. Outcomes [KDIGO], 2012). Post-Renal In the United States, AKI has grown by 14% annually since Obstruction of the urinary tract leading to increase pressure 2001, with approximately 5% to 25% of all hospitalized in the Bowman’s capsule and reduced glomerular filtration patients diagnosed with AKI (Brown, Rezaee, Marshall, & rate (GFR) caused by: Matheny, 2016). AKI is associated with high mortality rates. • Enlarged prostate. The number of AKI hospital-related deaths increased • Cancer of bladder, cervix, or prostate. almost twofold, from 147,943 deaths in 2001 to 285,768 • Blood clot (thrombus). deaths in 2011 (Brown et al., 2016). Patients who develop • Kidney stones (renal calculi). AKI are at risk for adverse outcomes, such as cardiovascu- • Urethral strictures. lar events, pulmonary complications, and end stage renal disease (ESRD); however, it is important to note that Risk Factors Associated with AKI approximately 66% of all AKI episodes develop in the com- • Advanced age. munity, outside of the hospital setting (Harty, 2014). • Surgical procedures, especially cardiovascular surgery. Therefore, prevention, early recognition, and management • Sepsis. are essential to decrease poor health outcomes associated • Major trauma resulting in blood loss and muscle dam- with AKI. age. • Multiple organ dysfunction syndrome (MODS) seen in Causes and Risk Factors critically ill patients. • Exposure to radiocontrast agents. The etiologies of AKI are multifactorial and categorized as • Nephrotoxic drugs (NSAIDs, methotrexate, ACE pre-renal, intra-renal, or post-renal (Lameire, Van Biesen, & inhibitors). Vanholder, 2005). • Dehydration. Pre-Renal Signs and Symptoms Reversible kidney hypoperfusion associated with: • Hypotension. The clinical presentation of patients with AKI vary depend- • Volume depletion due to hemorrhage, diarrhea, dehy- ing on the severity and cause of AKI (Rahman, Shad, & dration, severe burns, or diuretics. Smith, 2012). Many patients with mild or moderate AKI are • Organ failure, such as pancreatitis and liver disease, asymptomatic (Rahman et al., 2012). According to the which causes shift of fluid in the abdomen. National Kidney Foundation (2019), patients with more • Heart failure or heart attack. severe AKI may have the following symptoms: • Severe allergic reactions. • Jugular venous distention. Acute Kidney Injury Fact Sheet Clinical Issues • Edema (peripheral, periorbital). increases, allowing plateau of the BUN and creatinine, • Dyspnea. then a gradual decline. Although significant improvement • Nausea and vomiting. in kidney function is observed in the first 1 to 2 weeks of • Fatigue. this phase, it may take up to 12 months for kidney func- • Confusion. tion to stabilize. Some patients do not recover and • Chest pain or pressure. progress to ESRD. The outcome of AKI is contingent • Back pain. upon the patient’s overall health, the severity of kidney • Decreased urine output (oliguria). damage, and the presence of complications and comor- • Seizure or coma in severe cases. bid conditions. With aggressive treatment, most patients achieve normal kidney function without complications. There are four phases of AKI. Depending on the phase of AKI, other clinical manifestations of AKI often present in crit- Diagnosis and Evaluation ically ill patients, including metabolic acidosis, hyperkalemia, hypophosphatemia, uremia, and azotemia. Although the The diagnosis of AKI is multifactorial, with an emphasis on severity of symptoms and the complexity of renal dysfunc- identifying the underlying cause. History and physical tion vary, the clinical course and manifestations of AKI gen- examination are important components in the diagnosis of erally progress over the following four phases (Dirkes, 2015; AKI, including assessment of volume status (Rhaman et al., Lewis, Dirksen, Heikemper, Bucher, & Harding, 2014): 2012). When conducting the physical examination, assess- • Onset Phase: Initial insult to kidney due to factors such ment of intravascular volume status and skin rash, which as blood loss, dehydration, burns, diabetes insipidos, or indicates systemic illness, is essential (Rahman et al., 2012). infection, resulting in a decrease in renal blood flow and Initial laboratory studies to assist in identifying the cause of tissue oxygenation 25% of normal and urine output less AKI include complete blood count, urinalysis, and kidney than 0.5 mL/kg/hr. This phase last hours to days. function studies, such as measurement of serum creatinine, • Oliguric Phase: The most common initial clinical mani- BUN, and fractional excretion of sodium (Rahman et al., festation of AKI is oliguria, defined as a reduction in urine 2012). According to Workeneh, Agraharkar, and Gupta output less than 400 mL/day. Oliguria is manifested with- (2017), the following laboratory and diagnostic studies are in 1 to 7 days of kidney injury. This phase typically lasts often performed to diagnose and determine the cause of 10 to 14 days but can last months in some cases. The AKI: longer the oliguric phase, the poorer the prognosis for • BUN and Creatinine: Elevation of creatinine and BUN the recovery of kidney function. However, approximately are hallmark indicators of kidney injury. The BUN-to-cre- 50% of patients will not experience oliguria, making diag- atinine ratio can exceed 20:1 in conditions that promote nosis difficult. In the oliguric phase, signs of fluid volume reabsorption of urea, such as large volume loss, which overload, such as edema, distended neck veins, hyper- suggests pre-renal AKI. tension, pulmonary edema, and heart failure, may occur. • Complete Blood Count: Used to detect infection, In addition to signs of volume overload, metabolic acido- chronic anemia, blood loss, or thrombotic microan- sis, hyperkalemia, hyperphosphatemia, and uremic giopathy. symptoms may also be present. • Urinalysis: Muddy, brown, granular casts; oxalate crys- • Diuretic Phase: In this phase, daily urine output is tals; and tubular casts in urine sediment may indicate approximately 1 to 3 liters but can reach as high as 5 acute tubular necrosis (ATN). Urine that is reddish-brown liters or more. The kidneys recover their ability to excrete in color indicates myoglobinuria or hemoglobinuria. waste but cannot concentrate the urine. Hypovolemia Further, renal tubular injury will result in proteinuria. and hypotension may occur due to massive volume Urinary red blood cells (RBCs) occur due to bleeding loss. Due to the loss of large volumes of fluid and elec- along the collecting system. RBC casts or dysmorphic trolytes, patients should be monitored for hyponatremia, RBCs in the urine are the result of glomerular inflamma- hypokalemia, and dehydration. This phase may last 1 to tion or glomerulonephritis. The presence of white blood 3 weeks. During the end of this phase, fluid and elec- cells (WBCs) or WBC casts suggests pyelonephritis or trolytes, acid-base balance, and waste product values interstitial nephritis. (blood urea nitrogen [BUN] and creatinine) start to nor- • Peripheral Smear: The presence of schistocytes sug- malize. gests hemolytic uremic syndrome and thrombotic • Recovery Phase: This phase begins when the GFR thrombocytopenic purpura. 2 Acute Kidney Injury Fact Sheet Clinical Issues Table 1. Staging of AKI Stage Serum Creatinine Urine Output 1 1.5 to 1.9 times baseline < 0.5 mL/kg/h for 6 to 12 hours OR ≥ 0.3 mg/dL (≥ 26.5 mmol/l) increase 2 2.0 to 2.9 times baseline < 0.5 mL/kg/h for ≥ 12 hours 3 3.0 times baseline < 0.3 mL/kg/h for X 24 hours OR OR Increase in serum creatinine to ≥ 4.0 mg/dL (≥ 353.6 mmol/L) Anuria for X 12 hours OR Initiation of renal replacement therapy OR In patients <18 years, decrease in eGFR to < 35 mL/min/1.73 m2 Source: KDIGO, 2012. • Fraction of Urinary Sodium (FENa): Measures the identified AKI when serum creatinine levels remained within percent of sodium excreted in the urine and is used to the normal range (Bongiovanni et al., 2015). determine pre-renal vs. ATN as the cause of AKI. This test is useful only in the presence of oliguria. In pre-renal KDIGO (2012) makes the following recommenda- conditions, FENa is usually less than 1%. In ATN, the tions for patients at risk for AKI: FENa is typically greater
Recommended publications
  • Point-Of-Care Ultrasound to Assess Anuria in Children
    CME REVIEW ARTICLE Point-of-Care Ultrasound to Assess Anuria in Children Matthew D. Steimle, DO, Jennifer Plumb, MD, MPH, and Howard M. Corneli, MD patients to stay abreast of the most current advances in medicine Abstract: Anuria in children may arise from a host of causes and is a fre- and provide the safest, most efficient, state-of-the-art care. Point- quent concern in the emergency department. This review focuses on differ- of-care US can help us meet this goal.” entiating common causes of obstructive and nonobstructive anuria and the role of point-of-care ultrasound in this evaluation. We discuss some indications and basic techniques for bedside ultrasound imaging of the CLINICAL CONSIDERATIONS urinary system. In some cases, as for example with obvious dehydration or known renal failure, anuria is not mysterious, and evaluation can Key Words: point-of-care ultrasound, anuria, imaging, evaluation, be directed without imaging. In many other cases, however, diagnosis point-of-care US can be a simple and helpful way to assess urine (Pediatr Emer Care 2016;32: 544–548) volume, differentiate urinary retention in the bladder from other causes, evaluate other pathology, and, detect obstructive causes. TARGET AUDIENCE When should point-of-care US be performed? Because this imag- ing is low-risk, and rapid, early use is encouraged in any case This article is intended for health care providers who see chil- where it might be helpful. Scanning the bladder first answers the dren and adolescents in acute care settings. Pediatric emergency key question of whether urine is present.
    [Show full text]
  • Hemorrhagic Anuria with Acute Kidney Injury After a Single Dose of Acetazolamide: a Case Study of a Rare Side Effect
    Open Access Case Report DOI: 10.7759/cureus.10107 Hemorrhagic Anuria With Acute Kidney Injury After a Single Dose of Acetazolamide: A Case Study of a Rare Side Effect Christy Lawson 1 , Leisa Morris 2 , Vera Wilson 3 , Bracken Burns Jr 4 1. Surgery, Quillen College of Medicine, East Tennesse State University, Johnson City, USA 2. Trauma, Ballad Health Trauma Services, Johnson City, USA 3. Pharmacy, Ballad Health Trauma Services, Johnson City, USA 4. Surgery, Quillen College of Medicine, East Tennessee State University, Johnson City, USA Corresponding author: Bracken Burns Jr, [email protected] Abstract Acetazolamide (ACZ) is a relatively commonly used medication in critical illness, glaucoma and altitude sickness. ACZ is sometimes used in the intensive care unit to assist with the treatment of metabolic alkalosis in ventilated patients. This is a case report of a patient who received two doses of ACZ, one week apart, for metabolic alkalosis and subsequently developed renal colic and dysuria that progressed to hemorrhagic anuria and acute kidney injury. This is an incredibly rare side effect of ACZ therapy, and has been reported in a few case reports in the literature, but usually is associated with a longer duration of therapy. This case resolved entirely within 24 hours with aggressive fluid therapy. Clinicians using ACZ therapy for any reason should be aware of this rare but significant side effect. Categories: Trauma Keywords: acetazolamide, hemorrhagic anuria, acute kidney injury Introduction Acetazolamide (ACZ) is a carbonic anhydrase inhibitor. It works to cause an accumulation of carbonic acid in the proximal kidney, preventing its breakdown, and causes lowering of blood pH and resorption of sodium, bicarbonate, and chloride with their subsequent excretion into the urine [1].
    [Show full text]
  • Guidelines for Management of Acute Renal Failure (Acute Kidney Injury)
    Guidelines for management of Acute Renal Failure (Acute Kidney Injury) Children’s Kidney Centre University Hospital of Wales Cardiff CF14 4XW DISCLAIMER: These guidelines were produced in good faith by the author(s) reviewing available evidence/opinion. They were designed for use by paediatric nephrologists at the University Hospital of Wales, Cardiff for children under their care. They are neither policies nor protocols but are intended to serve only as guidelines. They are not intended to replace clinical judgment or dictate care of individual patients. Responsibility and decision-making (including checking drug doses) for a specific patient lie with the physician and staff caring for that particular patient. Version 1, S. Hegde/Feb 2009 Guidelines on management of Acute Renal Failure (Acute Kidney Injury) Definition of ARF (now referred to as AKI) • Acute renal failure is a sudden decline in glomerular filtration rate (usually marked by rise in serum creatinine & urea) which is potentially reversible with or without oliguria. • Oliguria defined as urine output <300ml/m²/day or < 0.5 ml/kg/h (<1 ml/kg/h in neonates). • Acute on chronic renal failure suggested by poor growth, history of polyuria and polydipsia, and evidence of renal osteodystrophy However, immediately after a kidney injury, serum creatinine & urea levels may be normal, and the only sign of a kidney injury may be decreased urine production. A rise in the creatinine level can result from medications (e.g., cimetidine, trimethoprim) that inhibit the kidney’s tubular secretion. A rise in the serum urea level can occur without renal injury, such as in GI or mucosal bleeding, steroid use, or protein loading.
    [Show full text]
  • Current Current
    CP_0406_Cases.final 3/17/06 2:57 PM Page 67 Current p SYCHIATRY CASES THAT TEST YOUR SKILLS Chronic enuresis has destroyed 12-year-old Jimmy’s emotional and social functioning. The challenge: restore his self-esteem by finding out why can’t he stop wetting his bed. The boy who longed for a ‘dry spell’ Tanvir Singh, MD Kristi Williams, MD Fellow, child® Dowdenpsychiatry ResidencyHealth training Media director, psychiatry Medical University of Ohio, Toledo CopyrightFor personal use only HISTORY ‘I CAN’T FACE MYSELF’ during regular checkups and refer to a psychia- immy, age 12, is referred to us by his pediatri- trist only if the child has an emotional problem J cian, who is concerned about his “frequent secondary to enuresis or a comorbid psychiatric nighttime accidents.” His parents report that he wets disorder. his bed 5 to 6 times weekly and has never stayed con- Once identified, enuresis requires a thorough sistently dry for more than a few days. assessment—including its emotional conse- The accidents occur only at night, his parents quences, which for Jimmy are significant. In its say. Numerous interventions have failed, including practice parameter for treating enuresis, the restricting fluids after dinner and awakening the boy American Academy of Child and Adolescent overnight to make him go to the bathroom. Psychiatry (AACAP)1 suggests that you: Jimmy, a sixth-grader, wonders if he will ever Take an extensive developmental and family stop wetting his bed. He refuses to go to summer history. Find out if the child was toilet trained and camp or stay overnight at a friend’s house, fearful started walking, talking, or running at an appro- that other kids will make fun of him after an acci- priate age.
    [Show full text]
  • Impact of Urolithiasis and Hydronephrosis on Acute Kidney Injury in Patients with Urinary Tract Infection
    bioRxiv preprint doi: https://doi.org/10.1101/2020.07.13.200337; this version posted July 13, 2020. The copyright holder for this preprint (which was not certified by peer review) is the author/funder, who has granted bioRxiv a license to display the preprint in perpetuity. It is made available under aCC-BY 4.0 International license. Impact of urolithiasis and hydronephrosis on acute kidney injury in patients with urinary tract infection Short title: Impact of urolithiasis and hydronephrosis on AKI in UTI Chih-Yen Hsiao1,2, Tsung-Hsien Chen1, Yi-Chien Lee3,4, Ming-Cheng Wang5,* 1Division of Nephrology, Department of Internal Medicine, Ditmanson Medical Foundation Chia-Yi Christian Hospital, Chia-Yi, Taiwan 2Department of Hospital and Health Care Administration, Chia Nan University of Pharmacy and Science, Tainan, Taiwan 3Department of Internal Medicine, Fu Jen Catholic University Hospital, Fu Jen Catholic University, New Taipei, Taiwan 4School of Medicine, College of Medicine, Fu Jen Catholic University, New Taipei, Taiwan 5Division of Nephrology, Department of Internal Medicine, National Cheng Kung University Hospital, College of Medicine, National Cheng Kung University, Tainan, Taiwan *[email protected] 1 bioRxiv preprint doi: https://doi.org/10.1101/2020.07.13.200337; this version posted July 13, 2020. The copyright holder for this preprint (which was not certified by peer review) is the author/funder, who has granted bioRxiv a license to display the preprint in perpetuity. It is made available under aCC-BY 4.0 International license. Abstract Background: Urolithiasis is a common cause of urinary tract obstruction and urinary tract infection (UTI). This study aimed to identify whether urolithiasis with or without hydronephrosis has an impact on acute kidney injury (AKI) in patients with UTI.
    [Show full text]
  • Uremic Toxins Affect Erythropoiesis During the Course of Chronic
    cells Review Uremic Toxins Affect Erythropoiesis during the Course of Chronic Kidney Disease: A Review Eya Hamza 1, Laurent Metzinger 1,* and Valérie Metzinger-Le Meuth 1,2 1 HEMATIM UR 4666, C.U.R.S, Université de Picardie Jules Verne, CEDEX 1, 80025 Amiens, France; [email protected] (E.H.); [email protected] (V.M.-L.M.) 2 INSERM UMRS 1148, Laboratory for Vascular Translational Science (LVTS), UFR SMBH, Université Sorbonne Paris Nord, CEDEX, 93017 Bobigny, France * Correspondence: [email protected]; Tel.: +33-2282-5356 Received: 17 July 2020; Accepted: 4 September 2020; Published: 6 September 2020 Abstract: Chronic kidney disease (CKD) is a global health problem characterized by progressive kidney failure due to uremic toxicity and the complications that arise from it. Anemia consecutive to CKD is one of its most common complications affecting nearly all patients with end-stage renal disease. Anemia is a potential cause of cardiovascular disease, faster deterioration of renal failure and mortality. Erythropoietin (produced by the kidney) and iron (provided from recycled senescent red cells) deficiencies are the main reasons that contribute to CKD-associated anemia. Indeed, accumulation of uremic toxins in blood impairs erythropoietin synthesis, compromising the growth and differentiation of red blood cells in the bone marrow, leading to a subsequent impairment of erythropoiesis. In this review, we mainly focus on the most representative uremic toxins and their effects on the molecular mechanisms underlying anemia of CKD that have been studied so far. Understanding molecular mechanisms leading to anemia due to uremic toxins could lead to the development of new treatments that will specifically target the pathophysiologic processes of anemia consecutive to CKD, such as the newly marketed erythropoiesis-stimulating agents.
    [Show full text]
  • The Links Between Microbiome and Uremic Toxins in Acute Kidney Injury: Beyond Gut Feeling—A Systematic Review
    toxins Article The Links between Microbiome and Uremic Toxins in Acute Kidney Injury: Beyond Gut Feeling—A Systematic Review Alicja Rydzewska-Rosołowska 1,* , Natalia Sroka 1, Katarzyna Kakareko 1, Mariusz Rosołowski 2 , Edyta Zbroch 1 and Tomasz Hryszko 1 1 2nd Department of Nephrology and Hypertension with Dialysis Unit, Medical University of Białystok, 15-276 Białystok, Poland; [email protected] (N.S.); [email protected] (K.K.); [email protected] (E.Z.); [email protected] (T.H.) 2 Department of Gastroenterology and Internal Medicine, Medical University of Białystok, 15-276 Białystok, Poland; [email protected] * Correspondence: [email protected] Received: 30 October 2020; Accepted: 9 December 2020; Published: 11 December 2020 Abstract: The last years have brought an abundance of data on the existence of a gut-kidney axis and the importance of microbiome in kidney injury. Data on kidney-gut crosstalk suggest the possibility that microbiota alter renal inflammation; we therefore aimed to answer questions about the role of microbiome and gut-derived toxins in acute kidney injury. PubMed and Cochrane Library were searched from inception to October 10, 2020 for relevant studies with an additional search performed on ClinicalTrials.gov. We identified 33 eligible articles and one ongoing trial (21 original studies and 12 reviews/commentaries), which were included in this systematic review. Experimental studies prove the existence of a kidney-gut axis, focusing on the role of gut-derived uremic toxins and providing concepts that modification of the microbiota composition may result in better AKI outcomes. Small interventional studies in animal models and in humans show promising results, therefore, microbiome-targeted therapy for AKI treatment might be a promising possibility.
    [Show full text]
  • Topic Objectives Physical Examination
    LECTURE MODULE 3; PHYSICAL EXAMINATION OF URINE Topic Objectives 1. Identify the colors which commonly associated with abnormal urine. 2. State two possible causes for urine turbidity in a sample that is not fresh. 3. Identify possible causes for abnormal urinary foam. 4. Identify the odors commonly associated with abnormal urine. 5. Differentiate between the following abnormalities of urine volume: Polyuria Oliguria Anuria Nocturia 6. Define specific gravity of urine. 7. Define refractive index of a solution. 8. Identify possible causes of abnormal specific gravities of urine. 9. Compare and contrast Diabetes Mellitus with Diabetes Insipidus. Physical Examination Appearance Color Transparency Foam Odor Specific Gravity Volume 1 Color • When an examiner first receives a urine specimen, color is observed and recorded. • Normal urine usually ranges from a light yellow to a dark amber color. • The normal metabolic products which are excreted from the body contribute to this color. • Urochrome is the chief urinary pigment. • Urinary color may vary, depending on concentration, dietary pigments, drugs, metabolites, and the presence or absence of blood. • A pale color generally indicates dilute urine with low specific gravity. • Occasionally, a pale urine with high specific gravity is seen in a diabetic patient. Color In many diseases, urinary color may drastically change. In liver disease, bile pigments may produce a yellow-brown or greenish tinge in the urine. Pink, red, or brown urine usually indicates the presence of blood, but porphyrins may also cause a pink or red urine. Since drugs, dyes and certain foods may alter urine color, the patient’s drug list and diet intake should be checked.
    [Show full text]
  • Full Text (PDF)
    www.jasn.org EDITORIALS 5. Grimm PR, Coleman R, Delpire E, Welling PA: Constitutively active Cachexia with muscle wasting is prevalent and closely associated SPAK causes hyperkalemia by activating NCC and remodeling distal with mortality and morbidity in patients with CKD.1 The patho- – tubules. JAmSocNephrol28: 2597 2606, 2017 physiology of muscle wasting in CKD is complex. Inadequate 6. Moriguchi T, Urushiyama S, Hisamoto N, Iemura S, Uchida S, Natsume T, Matsumoto K, Shibuya H: WNK1 regulates phosphorylation of cation- nutritional intake, physical inactivity from muscle weakness, sys- chloride-coupled cotransporters via the STE20-related kinases, SPAK temic inflammation and aberrant signaling of neuropeptides have and OSR1. J Biol Chem 280: 42685–42693, 2005 been implicated.2 To date, there is no effective therapy. Exercise 7. YangSS,MorimotoT,RaiT,ChigaM,SoharaE,OhnoM,UchidaK,LinSH, training has well documented health benefits, including mainte- Moriguchi T, Shibuya H, Kondo Y, SasakiS,UchidaS:Molecularpatho- nance of muscle mass as well as increased physical performance genesis of pseudohypoaldosteronism type II: Generation and analysis of a fi Wnk4(D561A/1) knockin mouse model. Cell Metab 5: 331–344, 2007 resulting from changes in muscle ber phenotype leading to in- 8. Lalioti MD, Zhang J, Volkman HM, Kahle KT, Hoffmann KE, Toka HR, Nelson- creased mitochondrial biogenesis. The molecular signaling mech- Williams C, Ellison DH, Flavell R, Booth CJ, Lu Y, Geller DS, Lifton RP: Wnk4 anism underlying adaptations to increased physical activity in controls blood pressure and potassium homeostasis via regulation of mass CKD-associated muscle wasting is not well understood. – and activity of the distal convoluted tubule.
    [Show full text]
  • Urinary System Diseases and Disorders
    URINARY SYSTEM DISEASES AND DISORDERS BERRYHILL & CASHION HS1 2017-2018 - CYSTITIS INFLAMMATION OF THE BLADDER CAUSE=PATHOGENS ENTERING THE URINARY MEATUS CYSTITIS • MORE COMMON IN FEMALES DUE TO SHORT URETHRA • SYMPTOMS=FREQUENT URINATION, HEMATURIA, LOWER BACK PAIN, BLADDER SPASM, FEVER • TREATMENT=ANTIBIOTICS, INCREASE FLUID INTAKE GLOMERULONEPHRITIS • AKA NEPHRITIS • INFLAMMATION OF THE GLOMERULUS • CAN BE ACUTE OR CHRONIC ACUTE GLOMERULONEPHRITIS • USUALLY FOLLOWS A STREPTOCOCCAL INFECTION LIKE STREP THROAT, SCARLET FEVER, RHEUMATIC FEVER • SYMPTOMS=CHILLS, FEVER, FATIGUE, EDEMA, OLIGURIA, HEMATURIA, ALBUMINURIA ACUTE GLOMERULONEPHRITIS • TREATMENT=REST, SALT RESTRICTION, MAINTAIN FLUID & ELECTROLYTE BALANCE, ANTIPYRETICS, DIURETICS, ANTIBIOTICS • WITH TREATMENT, KIDNEY FUNCTION IS USUALLY RESTORED, & PROGNOSIS IS GOOD CHRONIC GLOMERULONEPHRITIS • REPEATED CASES OF ACUTE NEPHRITIS CAN CAUSE CHRONIC NEPHRITIS • PROGRESSIVE, CAUSES SCARRING & SCLEROSING OF GLOMERULI • EARLY SYMPTOMS=HEMATURIA, ALBUMINURIA, HTN • WITH DISEASE PROGRESSION MORE GLOMERULI ARE DESTROYED CHRONIC GLOMERULONEPHRITIS • LATER SYMPTOMS=EDEMA, FATIGUE, ANEMIA, HTN, ANOREXIA, WEIGHT LOSS, CHF, PYURIA, RENAL FAILURE, DEATH • TREATMENT=LOW NA DIET, ANTIHYPERTENSIVE MEDS, MAINTAIN FLUIDS & ELECTROLYTES, HEMODIALYSIS, KIDNEY TRANSPLANT WHEN BOTH KIDNEYS ARE SEVERELY DAMAGED PYELONEPHRITIS • INFLAMMATION OF THE KIDNEY & RENAL PELVIS • CAUSE=PYOGENIC (PUS-FORMING) BACTERIA • SYMPTOMS=CHILLS, FEVER, BACK PAIN, FATIGUE, DYSURIA, HEMATURIA, PYURIA • TREATMENT=ANTIBIOTICS,
    [Show full text]
  • Quantitative Micro-Computed Tomography Imaging of Vascular Dysfunction in Progressive Kidney Diseases
    BASIC RESEARCH www.jasn.org Quantitative Micro-Computed Tomography Imaging of Vascular Dysfunction in Progressive Kidney Diseases † †‡ † Josef Ehling,* Janka Bábícková, Felix Gremse,* Barbara M. Klinkhammer, † | Sarah Baetke,* Ruth Knuechel, Fabian Kiessling,* Jürgen Floege,§ Twan Lammers,* ¶ and †‡ Peter Boor § *Institute for Experimental Molecular Imaging, Helmholtz Institute for Biomedical Engineering, Medical Faculty, Rheinisch-Westfälische Technische Hochschule (RWTH) Aachen University, Aachen, Germany; †Institute of Pathology, Medical Faculty, RWTH Aachen University, Aachen, Germany; ‡Institute of Molecular Biomedicine, Comenius University, Bratislava, Slovakia; §Department of Nephrology, Medical Faculty, RWTH Aachen University, Aachen, Germany; |Department of Targeted Therapeutics, MIRA Institute for Biomedical Technology and Technical Medicine, University of Twente, Enschede, The Netherlands; and ¶Department of Pharmaceutics, Utrecht Institute for Pharmaceutical Sciences, Utrecht University, Utrecht, The Netherlands ABSTRACT Progressive kidney diseases and renal fibrosis are associated with endothelial injury and capillary rarefaction. However, our understanding of these processes has been hampered by the lack of tools enabling the quantitative and noninvasive monitoring of vessel functionality. Here, we used micro-computed tomography (mCT) for anatomical and functional imaging of vascular alterations in three murine models with distinct mechanisms of progressive kidney injury: ischemia-reperfusion (I/R, days 1–56), unilateral ureteral obstruction (UUO, days 1–10), and Alport mice (6–8 weeks old). Contrast-enhanced in vivo mCT enabled robust, non- invasive, and longitudinal monitoring of vessel functionality and revealed a progressive decline of the renal relative blood volume in all models. This reduction ranged from 220% in early disease stages to 261% in late disease stages and preceded fibrosis. Upon Microfil perfusion, high-resolution ex vivo mCT allowed quanti- tative analyses of three-dimensional vascular networks in all three models.
    [Show full text]
  • Synchrotron Microangiography Studies of Angiogenesis in Mice with Microemulsions and Gold Nanoparticles
    Anal Bioanal Chem (2010) 397:2109–2116 DOI 10.1007/s00216-010-3775-8 ORIGINAL PAPER Synchrotron microangiography studies of angiogenesis in mice with microemulsions and gold nanoparticles Chia-Chi Chien & C. H. Wang & C. L. Wang & E. R. Li & K. H. Lee & Y. Hwu & Chien-Yi Lin & Shing-Jyh Chang & C. S. Yang & Cyril Petibois & G. Margaritondo Received: 7 February 2010 /Revised: 17 April 2010 /Accepted: 22 April 2010 /Published online: 6 June 2010 # Springer-Verlag 2010 Abstract We present an effective solution for the problem provides the best contrast and minimal distortion of the of contrast enhancement in phase-contrast microangiogra- circulation and vessel structure. Such emulsions are phy, with the specific objective of visualising small reasonably biocompatible and, with sizes of 0±0.8 µm, (<8 µm) vessels in tumor-related microangiogenesis. sufficient to diffuse to the smallest vessel and still provide Different hydrophilic and hydrophobic contrast agents were reasonable contrast. We also explored the use of Au explored in this context. We found that an emulsified nanoparticle colloids that could be used not only to enhance version of the hydrophobic contrast agents Lipiodol® contrast but also for interesting applications in nano- medicine. Both the Lipiodol microemulsions and Au nanoparticle colloids can be conjugated with medicines or C.-C. Chien : C. H. Wang : C. L. Wang : E. R. Li : K. H. Lee : Y. Hwu (*) cell specific labeling agents and their small size can allow Institute of Physics, Academia Sinica, the study of the diffusion of contrast agents through the Nankang, vessel leakage. This enables direct imaging of drug delivery Taipei 115, Taiwan, China which is important for cancer treatment.
    [Show full text]